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991.
目的 研究扬子鳄(Alligator sinensis)消化道中生长素释放肽ghrelin免疫活性(IR)细胞的分布、组织定位及其在冬眠期的变化.方法 应用链霉亲和素-生物素-过氧化物酶复合物(SABC)免疫组织化学方法结合生物统计学分析.结果 Ghrelin-IR细胞在扬子鳄的小胃密度最高,在胃贲门部、胃体和胃幽门部有少量分布,主要位于胃腺上皮细胞之间.在食管、十二指肠、空肠、回肠和直肠中均未检测出ghrelin-IR细胞.冬眠期小胃ghrelin-IR细胞显著性减少(P〈0.01),其它部位无显著性变化(P〉0.05).结论扬子鳄消化道ghrelin-IR细胞的分布同其它动物有相似之处,也有其一定的特异性.Ghrelin在扬子鳄冬眠期的代谢变化和能量稳态的调节中起重要作用. 相似文献
992.
Zide Zhang Luyuan Huang Qiuhong Wu Enze Yang Guang Zhang Hanxiao Sun Feng Wang 《Molecular and cellular biochemistry》2014,385(1-2):79-86
Human manganese superoxide dismutase (hMnSOD) is a new type of cancer suppressor. Nonamer of arginine (R9) is an efficient protein transduction domain (PTD). The aim of the study was to improve the transduction efficiency of hMnSOD and investigate its activity in vitro. In this study, we designed, constructed, expressed, and purified a novel fusion protein containing the hMnSOD domain and R9 PTD (hMnSOD–R9). The DNA damaged by Fenton’s reagent was found to be significantly reduced when treated with hMnSOD–R9. hMnSOD–R9 fusion protein was successfully delivered into HeLa cells. The MTT assay showed that proliferation of various cancer cell lines were inhibited by hMnSOD–R9 in a dose-dependent manner. In addition, the cell cycle of HeLa cells was arrested at the sub-G0 phase by hMnSOD–R9. hMnSOD–R9 induced apoptosis of HeLa cells in a dose-dependent manner. With hMnSOD–R9 treatment, Bax, JNK, TBK1 gene expression was increased and STAT3 gene expression was gradually down-regulated in HeLa cells. We also found that apoptosis was induced by hMnSOD–R9 in HeLa cells via up-regulation of cleaved caspase-3 and down-regulation phospho-STAT3 pathway. These results indicated that hMnSOD–R9 may provide benefits to cervical cancer treatment. 相似文献
993.
Xiao-hong Cao Si-si Zhao Dong-yue Liu Zhuo Wang Li-li Niu Li-hua Hou Chun-ling Wang 《Chemico-biological interactions》2011,(1):16
The surfactin can inhibit proliferation and induce apoptosis in cancer cells. Moreover, surfactin can induce cell death in human breast cancer MCF-7 cells through mitochondrial pathway. However, the molecular mechanism involved in this pathway remains to be elucidated. Here, the reactive oxygen species (ROS) and Ca2+ on mitochondria permeability transition pore (MPTP) activity, and MCF-7 cell apoptosis which induced by surfactin were investigated. It is found that surfactin evoked mitochondrial ROS generation, and the surfactin-induced cell death was prevented by N-acetylcysteine (NAC, an inhibitor of ROS). An increasing cytoplasmic Ca2+ concentration was detected in surfactin-induced MCF-7 apoptosis, which was inhibited by 1,2-bis (2-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid (BAPTA-AM, a chelator of calcium). In addition, the relationship between ROS generation and the increase of cytoplasm Ca2+ was determined. The results showed that surfactin initially induced the ROS formation, leading to the MPTP opening accompanied with the collapse of mitochondrial membrane potential (ΔΨm). Then the cytoplasmic Ca2+ concentration increased in virtue of the changes of mitochondrial permeability, which was prevented by BAPTA-AM. Besides, cytochrome c (cyt c) was released from mitochondria to cytoplasm through the MPTP and activated caspase-9, eventually induced apoptosis. In summary, surfactin has notable anti-tumor effect on MCF-7 cells, however, there was no obvious cytotoxicity on normal cells. 相似文献
994.
995.
Differential role of microenvironment in microencapsulation for improved cell tolerance to stress 总被引:6,自引:0,他引:6
Sun ZJ Lv GJ Li SY Yu WT Wang W Xie YB Ma X 《Applied microbiology and biotechnology》2007,75(6):1419-1427
The effect of the microenvironment in alginate–chitosan–alginate (ACA) microcapsules with liquid core (LCM) and solid core
(SCM) on the physiology and stress tolerance of Sacchromyces cerevisiae was studied. The suspended cells were used as control. Cells cultured in liquid core microcapsules showed a nearly twofold
increase in the intracellular glycerol content, trehalose content, and the superoxide dismutase (SOD) activity, which are
stress tolerance substances, while SCM did not cause the significant physiological variation. In accordance with the physiological
modification after being challenged with osmotic stress (NaCl), oxidative stress (H2O2), ethanol stress, and heat shock stress, the cell survival in LCM was increased. However, SCM can only protect the cells
from damaging under ethanol stress. Cells released from LCM were more resistant to hyperosmotic stress, oxidative stress,
and heat shock stress than cells liberated from SCM. Based on reasonable analysis, a method was established to estimate the
effect of microenvironment of LCM and SCM on the protection of cells against stress factors. It was found that the resistance
of LCM to hyperosmotic stress, oxidative stress, and heat shock stress mainly depend on the domestication effect of LCM’s
microenvironment. The physical barrier of LCM constituted by alginate–chitosan membrane and liquid alginate matrix separated
the cells from the damage of oxidative stress and ethanol stress. The significant tolerance against ethanol stress of SCM
attributed to the physical barrier consists of solid alginate–calcium matrix and alginate–chitosan membrane. 相似文献
996.
Ye L Zhu W Backx PH Cortez MA Wu J Chow YH McKerlie C Wang A Tsui LC Gross GJ Hu J 《Journal of cellular and molecular medicine》2011,15(11):2307-2316
The identification and analysis of several cationic ion channels and their associated genes have greatly improved our understanding of the molecular and cellular mechanisms of cardiac arrhythmia. Our objective in this study was to examine the involvement of anionic ion channels in cardiac arrhythmia. We used a transgenic mouse model to overexpress the human cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes a cAMP-regulated chloride channel. We used RNase protection and in situ hybridization assays to determine the level of CFTR expression, and radiotelemetry and in vivo electrophysiological study in combination with pharmacological intervention to analyse the cardiac function. Cardiac CFTR overexpression leads to stress-related sudden death in this model. In vivo intracardiac electrophysiological studies performed in anaesthetized mice showed no significant differences in baseline conduction parameters including atrial-His bundle (AH) or His bundle-ventricular (HV) conduction intervals, atrioventricular (AV) Wenckebach or 2:1 AV block cycle length and AV nodal functional refractory period. However, following isoproterenol administration, there was marked slowing of conduction parameters, including high-grade AV block in transgenic mice, with non-sustained ventricular tachycardia easily inducible using programmed stimulation or burst pacing. Our sudden death mouse model can be a valuable tool for investigation of the role of chloride channels in arrhythmogenesis and, potentially, for future evaluation of novel anti-arrhythmic therapeutic strategies and pharmacological agents. 相似文献
997.
Zhang R Mayhood T Lipari P Wang Y Durkin J Syto R Gesell J McNemar C Windsor W 《Analytical biochemistry》2004,331(1):138-146
MDM2 is an important negative regulator of the tumor suppressor protein p53 which regulates the expression of many genes including MDM2. The delicate balance of this autoregulatory loop is crucial for the maintenance of the genome and control of the cell cycle and apoptosis. MDM2 hyperactivity, due to amplification/overexpression or mutational inactivation of the ARF locus, inhibits the function of wild-type p53 and can lead to the development of a wide variety of cancers. Thus, the development of anti-MDM2 therapies may restore normal p53 function in tumor cells and induce growth suppression and apoptosis. We report here a novel high-throughput fluorescence polarization binding assay and its application in rank ordering small-molecule inhibitors that block the binding of MDM2 to a p53-derived fluorescent peptide. 相似文献
998.
Ji-Fu Wei Xiao-long Wei Qiu-Yu Chen Tian Huang Li-Ya Qiao Wan-Yu Wang Yu-Liang Xiong Shao-Heng He 《Biochimica et Biophysica Acta (BBA)/General Subjects》2006
A novel phospholipase A2 (PLA2) with Asn at its site 49 was purified from the snake venom of Protobothrops mucrosquamatus by using SP-Sephadex C25, Superdex 75, Heparin-Sepharose (FF) and HPLC reverse-phage C18 chromatography and designated as TM-N49. It showed a molecular mass of 13.875 kDa on MALDI-TOF. TM-N49 does not possess enzymatic, hemolytic and hemorrhagic activities. It fails to induce platelet aggregation by itself, and does not inhibit the platelet aggregation induced by ADP. However, it exhibits potent myotoxic activity causing inflammatory cell infiltration, severe myoedema, myonecrosis and myolysis in the gastrocnemius muscles of BALB/c mice. Phylogenetic analysis found that that TM-N49 combined with two phospholipase A2s from Trimeresurus stejnegeri, TsR6 and CTs-R6 cluster into one group. Structural and functional analysis indicated that these phospholipase A2s are distinct from the other subgroups (D49 PLA2, S49 PLA2 and K49 PLA2) and represent a unique subgroup of snake venom group II PLA2, named N49 PLA2 subgroup. 相似文献
999.
Blockade of L-type voltage-gated Ca channel inhibits ischemia-induced neurogenesis by down-regulating iNOS expression in adult mouse 总被引:3,自引:0,他引:3
Luo CX Zhu XJ Zhang AX Wang W Yang XM Liu SH Han X Sun J Zhang SG Lu Y Zhu DY 《Journal of neurochemistry》2005,94(4):1077-1086
Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. The signals that regulate neurogenesis in the dentate gyrus following ischemic stroke insult are not well known. We have previously reported that inducible nitric oxide synthase (iNOS) expression is necessary for ischemia-stimulated neurogenesis in the adult dentate gyrus. Here, we show that mice subjected to 90 min of middle cerebral artery occlusion (MCAO) significantly increased the number of new neurons and up-regulated iNOS expression in the dentate gyrus. Blockade of the L-type voltage-gated Ca(2+) channel (L-VGCC) prevented neurogenesis in the dentate gyrus and subventricular zone (SVZ), and down-regulated iNOS expression in the dentate gyrus after cerebral ischemia. This study suggests that Ca(2+) influx through L-VGCC is involved in ischemia-induced neurogenesis by up-regulating iNOS expression. 相似文献
1000.
Novel Partial Reductive Pathway for 4-Chloronitrobenzene and Nitrobenzene Degradation in Comamonas sp. Strain CNB-1 总被引:3,自引:0,他引:3 下载免费PDF全文
Jian-feng Wu Cheng-ying Jiang Bao-jun Wang Ying-fei Ma Zhi-pei Liu Shuang-jiang Liu 《Applied microbiology》2006,72(3):1759-1765
Comamonas sp. strain CNB-1 grows on 4-chloronitrobenzene (4-CNB) and nitrobenzene as sole carbon and nitrogen sources. In this study, two genetic segments, cnbB-orf2-cnbA and cnbR-orf1-cnbCaCbDEFGHI, located on a newly isolated plasmid, pCNB1 (ca. 89 kb), and involved in 4-CNB/nitrobenzene degradation, were characterized. Seven genes (cnbA, cnbB, cnbCa, cnbCb, cnbD, cnbG, and cnbH) were cloned and functionally expressed in recombinant Escherichia coli, and they were identified as encoding 4-CNB nitroreductase (CnbA), 1-hydroxylaminobenzene mutase (CnbB), 2-aminophenol 1,6-dioxygenase (CnbCab), 2-amino-5-chloromuconic semialdehyde dehydrogenase (CnbD), 2-hydroxy-5-chloromuconic acid (2H5CM) tautomerase, and 2-amino-5-chloromuconic acid (2A5CM) deaminase (CnbH). In particular, the 2A5CM deaminase showed significant identities (31 to 38%) to subunit A of Asp-tRNAAsn/Glu-tRNAGln amidotransferase and not to the previously identified deaminases for nitroaromatic compound degradation. Genetic cloning and expression of cnbH in Escherichia coli revealed that CnbH catalyzed the conversion of 2A5CM into 2H5CM and ammonium. Four other genes (cnbR, cnbE, cnbF, and cnbI) were tentatively identified according to their high sequence identities to other functionally identified genes. It was proposed that CnbH might represent a novel type of deaminase and be involved in a novel partial reductive pathway for chloronitrobenzene or nitrobenzene degradation. 相似文献